ArticleThe EMBO journal2001
Rad52 partially substitutes for the Rad51 paralog XRCC3 in maintaining chromosomal integrity in vertebrate cells.
Article in The EMBO journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 132 citations in OpenAlex.
- Replication Protein A Phosphorylation Facilitates RAD52-Dependent Homologous Recombination in BRCA-Deficient Cells.Molecular and cellular biology · 2022Article
- Targeting the Homologous Recombination Pathway in Cancer With a Novel Class of RAD51 Inhibitors.Frontiers in oncology · 2022Article
- RAD52 Adjusts Repair of Single-Strand Breaks via Reducing DNA-Damage-Promoted XRCC1/LIG3α Co-localization.Cell reports · 2021Article
- Differential Requirements for the RAD51 Paralogs in Genome Repair and Maintenance in Human Cells.PLoS genetics · 2019Article
- Review
- Human somatic cells deficient for RAD52 are impaired for viral integration and compromised for most aspects of homology-directed repair.DNA repair · 2017Article
- The effects of pprI gene of Deinococcus radiodurans R1 on acute radiation injury of mice exposed to 60Co γ-ray radiation.Oncotarget · 2017Article
- Novel insights into RAD51 activity and regulation during homologous recombination and DNA replication.Biochemistry and cell biology = Biochimie et biologie cellulaire · 2016Review
- Review
- Targeting BRCA1- and BRCA2-deficient cells with RAD52 small molecule inhibitors.Nucleic acids research · 2016Article
- Accessory Factors of Cytoplasmic Viral RNA Sensors Required for Antiviral Innate Immune Response.Frontiers in immunology · 2016Review
- Cell biology of mitotic recombination.Cold Spring Harbor perspectives in biology · 2015Review
- Mediators of homologous DNA pairing.Cold Spring Harbor perspectives in biology · 2014Review
- Structure-specific endonucleases xpf and mus81 play overlapping but essential roles in DNA repair by homologous recombination.Cancer research · 2013Article
- Rad51 paralog complexes BCDX2 and CX3 act at different stages in the BRCA1-BRCA2-dependent homologous recombination pathway.Molecular and cellular biology · 2013Article
- DNA double-strand break repair as determinant of cellular radiosensitivity to killing and target in radiation therapy.Frontiers in oncology · 2013Article
- Molecular pathways: understanding the role of Rad52 in homologous recombination for therapeutic advancement.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012Review
- Homologous recombination and its regulation.Nucleic acids research · 2012Review
- Identification of plant RAD52 homologs and characterization of the Arabidopsis thaliana RAD52-like genes.The Plant cell · 2011Article
- Unraveling the mechanism of BRCA2 in homologous recombination.Nature structural & molecular biology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Yeast Rad52 DNA-repair mutants exhibit pronounced radiation sensitivity and a defect in homologous re combination (HR), whereas vertebrate cells lacking Rad52 exhibit a nearly normal phenotype. Bio chemical studies show that both yeast Rad52 and Rad55-57 (Rad51 paralogs) stimulate DNA-strand exchange mediated by Rad51. These findings raise the possibility that Rad51 paralogs may compensate for lack of Rad52 in vertebrate cells, explaining the absence of prominent phenotypes for Rad52-deficient cells. To test this hypothesis, using chicken DT40 cells, we generated conditional mutants deficient in both RAD52 and XRCC3, which is one of the five vertebrate RAD51 paralogs. Surprisingly, the rad52 xrcc3 double-mutant cells were non-viable and exhibited extensive chromosomal breaks, whereas rad52 and xrcc3 single mutants grew well. Our data reveal an overlapping (but non-reciprocal) role for Rad52 and XRCC3 in repairing DNA double-strand breaks. The present study shows that Rad52 can play an important role in HR repair by partially substituting for a Rad51 paralog.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.